ScienceDaily (Apr. 6, 2011) — A new pathway has been discovered that links a common dietary lipid and intestinal microflora with an increased risk of heart disease, according to a Cleveland Clinic study published in the latest issue of Nature.

The study shows that people who eat a diet containing a common nutrient found in animal products (such as eggs, liver and other meats, cheese and other dairy products, fish, shellfish) are not predisposed to cardiovascular disease solely on their genetic make-up, but rather, how the micro-organisms that live in our digestive tracts metabolize a specific lipid -- phosphatidyl choline (also called lecithin). Lecithin and its metabolite, choline, are also found in many commercial baked goods, dietary supplements, and even children's vitamins.

The study examined clinical data from 1,875 patients who were referred for cardiac evaluation, as well as plasma samples from mice. When fed to mice, lecithin and choline were converted to a heart disease-forming product by the intestinal microbes, which promoted fatty plaque deposits to form within arteries (atherosclerosis); in humans, higher blood levels of choline and the heart disease forming microorganism products are strongly associated with increased cardiovascular disease risk.

"When two people both eat a similar diet but one gets heart disease and the other doesn't, we currently think the cardiac disease develops because of their genetic differences; but our studies show that is only a part of the equation," said Stanley Hazen, M.D., Ph.D., Staff in Lerner Research Institute's Department of Cell Biology and the Heart and Vascular Institute's Department of Cardiovascular Medicine and Section Head of Preventive Cardiology & Rehabilitation at Cleveland Clinic, and senior author of the study. "Actually, differences in gut flora metabolism of the diet from one person to another appear to have a big effect on whether one develops heart disease. Gut flora is a filter for our largest environmental exposure -- what we eat."

Dr. Hazen added, "Another remarkable finding is that choline -- a natural semi-essential vitamin -- when taken in excess, promoted atherosclerotic heart disease. Over the past few years we have seen a huge increase in the addition of choline into multi-vitamins -- even in those marketed to our children -- yet it is this same substance that our study shows the gut flora can convert into something that has a direct, negative impact on heart disease risk by forming an atherosclerosis-causing by-product."

In studies of more than 2,000 subjects altogether, blood levels of three metabolites of the dietary lipid lecithin were shown to strongly predict risk for cardiovascular disease: choline (a B-complex vitamin), trimethylamine N-oxide (TMAO, a product that requires gut flora to be produced and is derived from the choline group of the lipid) and betaine (a metabolite of choline).

"The studies identify TMAO as a blood test that can be used in subjects to see who is especially at risk for cardiac disease, and in need of more strict dietary intervention to lower their cardiac risk," Dr. Hazen said.

Healthy amounts of choline, betaine and TMAO are found in many fruits, vegetables and fish. These three metabolites are commonly marketed as direct-to-consumer supplements, supposedly offering increased brain health, weight loss and/or muscle growth.

These compounds also are commonly used as feed additives for cattle, poultry or fish because they may make muscle grow faster; whether muscle from such livestock have higher levels of these compounds remains unknown.

"Knowing that gut flora generates a pro-atherosclerotic metabolite from a common dietary lipid opens up new opportunities for improved diagnostics, prevention and treatment of heart disease," Dr. Hazen said. "These studies suggest we can intelligently design a heart healthy yogurt or other form of probiotic for preventing heart disease in the future. It also appears there is a need for considering the risk vs. benefits of some commonly used supplements."

Too much of it will make you go blind – or so you might have been told. But for some, masturbation might have a real clinical benefit: it can ease restless leg syndrome (RLS). The insight could provide sweet relief for the 7 to 10 per cent of people in the US and Europe who suffer from the condition.RLS is a distressing neurologic disorder characterised by an urge to move the legs. It is usually associated with unpleasant sensations in the lower limbs such as tingling, aching and itching.The exact causes of RSL have yet to be pinpointed, but brain autopsies and imaging studies suggest one contributing factor is an imbalance of dopamine – a hormonal messenger that, among other things, activates the areas of the brain responsible for pleasure. It is suspected that dopamine imbalance is responsible for some of the symptoms of Parkinson's disease.Drugs that increase dopamine have been shown to reduce symptoms of RLS when taken at bedtime and are considered the initial treatment of choice.Although such drugs provided significant improvement of symptoms for a 41-year-old man with RLS, he found an even better treatment – complete relief after masturbation or sex.

An ingenious set of experiments has teased apart the mind-altering and pain-relieving effects of the main component of cannabis. This could open the way to cannabis-like drugs that provide pain relief without causing unwanted highs.

Cannabis is taken as a painkiller – to dull pain in cancer for example – but it can produce unpleasant side effects such as hallucinations and impaired mobility.

Now, a team led by Li Zhang of the US National Institute on Alcohol Abuse and Alcoholism in Bethesda, Maryland, has shown that tetrahydrocannabinol (THC) – the active component in cannabis that makes people high but that is also thought to dull pain – binds to different molecular targets on cells to produce these two effects.

It has long been known that THC gives people a high by binding to a molecular anchor on cells called the cannabinoid type-1 (CB1) receptor. Zhang and his team discovered that THC relieves pain by binding instead to receptors for the brain-signalling compound glycine and increasing their activity.

Through experiments on mice, they then confirmed that if the glycine receptor is absent or if its activity is blocked by another drug, the animals experienced pain in a standard "tail-flick" test even when given THC, confirming that the drug's pain-relief and psychotropic effects can be decoupled.